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1.

001-es BibID:BIBFORM041686
Első szerző:Abrahám Csongor
Cím:Adrenalectomy aggravates ischemic brain edema in female Sprague-Dawley rats with carotid arteries ligated / Cs. Abrahám, M. Koltai, F. Joó, Á. Tósaki, P. Szerdahelyi
Dátum:1992
ISSN:0079-6123
Megjegyzések:The effect of adrenalectomy has been investigated in a model of global cerebral ischemia. After bilateral carotid ligation the mortality rate was increased in adrenalectomized rats, and this effect was prevented by glucocorticoid pre-treatment. Adrenalectomy accelerated the appearance of the symptoms of cerebral ischemia, resulting in a moderate aggravation of brain edema and in a significant decrease in the concentration of high-energy phosphate esters. Our findings support the view that endogenous glucocorticoids may play a role in the amelioration of ischemic brain injuries in rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Progress in Brain Research. - 91 (1992), p. 23-27. -
További szerzők:Koltai Mátyás Joó F. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szerdahelyi Péter
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2.

001-es BibID:BIBFORM042021
Első szerző:Ferdinándy Péter
Cím:Cicletanine improves myocardial function deteriorated by ischemia/reperfusion in isolated working rat hearts / Ferdinandy Péter, Koltai Mátyás, Tósaki Árpád, Berthet Philippe, Tarrade Thierry, Esanu André, Braquet Pierre
Dátum:1992
Megjegyzések:The effect of cicletanine, a novel furopyridine antihypertensive drug was compared with that of nitrendipine, a dihydropyridine slow calcium channel blocker, on cardiac function and reperfusion-induced ventricular arrhythmias in isolated working rat hearts subjected to 10-min ischemia induced by ligation of the left main coronary artery followed by 10-min reperfusion. Before ischemia, cicletanine and nitrendipine, perfused at concentrations of 3 x 10(-5), 6 x 10(-5), 10(-4), and 2 x 10(-4) or 10(-8) M, respectively, did not influence heart rate (HR), LV developed pressure (LVDP), its first derivative (LVdP/dtmax), and LV end-diastolic pressure (LVEDP), whereas aortic flow (AF) was decreased by 2 x 10(-4) M cicletanine only. Coronary flow (CF) remained unchanged by various cicletanine concentrations but was slightly increased by nitrendipine. In the concentration range of 3 x 10(-5)-10(-4) M, cicletanine improved AF either in ischemia or during reperfusion, whereas 2 x 10(-4) M had no such effect. Nitrendipine slightly attenuated ischemia/reperfusion-induced decrease in AF. Cicletanine and nitrendipine enhanced LVDP during ischemia. Ischemia-induced deterioration of LVdP/dtmax was reduced by cicletanine, during reperfusion, but this parameter was reduced by nitrendipine and the highest cicletanine concentration. Cicletanine decreased LVEDP significantly during ischemia and reperfusion, but nitrendipine had no such effect. All cicletanine concentrations reduced the incidence of irreversible ventricular fibrillation (VF) during reperfusion, an effect roughly concentration dependent in the range of 3 x 10(-5)-10(-4) M, whereas nitrendipine had no influence on arrhythmias.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 19 : 2 (1992), p. 181-189. -
További szerzők:Koltai Mátyás Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Berthet, Philippe Tarrade, Thierry Esanu, Andre Braquet, Pierre
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3.

001-es BibID:BIBFORM041648
035-os BibID:PMID:2758320
Első szerző:Joó Ferenc (vegyész)
Cím:Inhibition by H-7 of the protein kinase C prevents formation of brain edema in Sprague-Dawley CFY rats / Ferenc Joó, Árpád Tósaki, Zoltán Oláh, Mátyás Koltai
Dátum:1989
Megjegyzések:The effect of the protein kinase C enzyme inhibitor H-7 was examined on the brain edema formation evoked by bilateral occlusion of the common carotid arteries in Sprague-Dawley rats of CFY strain. Brain edema was assessed by measurement of water and electrolyte contents of the brain. The results showed that pretreatment with H-7 reduced the extent of brain edema formation in a dose-dependent manner. The fact that H-7 treatment prevented the accumulation of water and certain electrolytes in the brain indicates that the protein kinase C may be activated not only in the neuronal structures but also in the microvessels during ischemia, which can lead directly or via certain calcium-mediated mechanisms to the opening of tight junctions resulting in the development of brain edema.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Brain Research 490 : 1 (1989), p. 141-143. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Oláh Zoltán Koltai Mátyás
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4.

001-es BibID:BIBFORM041688
Első szerző:Koltai Mátyás
Cím:Effect of cicletanine on reperfusion-induced arrhythmias and myocardial ion contents : a comparison with furosemid / Koltai M., Tosaki A., Berthet P., Tarrade T., Esanu A., Braquet P.
Dátum:1992
Megjegyzések:We studied the effects of cicletanine, a furopyridine antihypertensive drug, and furosemide, a loop diuretic, on ventricular arrhythmias, such as sustained ventricular fibrillation (VF) and ventricular tachycardia (VT), and myocardial ion content in Langendorff rat hearts subjected to 30 min global ischaemia then 10 min reperfusion. Myocardial Na+, K+, Ca2+ and Mg2+ concentrations were measured by washout technique and atomic absorption spectrophotometry before and after ischaemia and reperfusion. Drugs were either perfused (acute treatment) or orally gavaged daily to the rats for 14 days before isolation of their hearts (chronic treatment). Under in vitro conditions 10(-5), 3 x 10(-5), 10(-4) or 3 x 10(-4) M of cicletanine reduced the incidence of sustained VF and VT from the control values of 91% and 100% to 83% and 100%, 50% (P less than 0.05) and 67%, 33% (P less than 0.01) and 50% (P less than 0.05), 25% (P less than 0.01) and 41% (P less than 0.05), respectively. Chronic treatment with 3, 10, 30 or 100 mg.kg-1.day-1 of cicletanine also resulted in a dose-dependent anti-arrhythmic effect. Neither acute (10(-5), 3 x 10(-5) and 10(-4) M) nor chronic furosemide treatment (3, 10 and 30 mg.kg-1.day-1) influenced the incidence of arrhythmias. Acute treatment with cicletanine or furosemide did not change myocardial ion concentrations, in non-ischaemic hearts, while chronic treatment with 30 mg.kg-1.day-1 furosemide significantly reduced myocardial Na+, K+ and Mg2+ content and increased Ca2+ concentration. Both acute and chronic cicletanine treatments attenuated ischaemia/reperfusion-induced myocardial Na+ and Ca2+ gains and K+ loss, while furosemide did not
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Heart Journal. - 13 : 3 (1992), p. 395-403. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Berthet, P. Tarrade, T. Esanu, Andre Braquet, Pierre
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5.

001-es BibID:BIBFORM041685
Első szerző:Koltai Mátyás
Cím:Cicletanine : a novel approach to cardioprotection in spontaneously hypertensive rats / Matyas Koltai, Arpad Tosaki, Thierry Tarrade, Philippe Berthet, Andre Esanu, Pierre G. Braquet
Dátum:1991
ISSN:0954-6928
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Coronary Artery Disease. - 2 (1991), p. 941-944. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Tarrade, Thierry Berthet, Philippe Esanu, Andre Braquet, Pierre
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6.

001-es BibID:BIBFORM041684
Első szerző:Koltai Mátyás
Cím:Effect of BN 50739, a new platelet activating factor antagonist, on ischaemia induced ventricular arrhythmias in isolated working rat hearts / Koltai M., Tosaki A., Hosford D., Esanu A., Braquet P.
Dátum:1991
ISSN:0008-6363
Megjegyzések:STUDY OBJECTIVE: The aim was to investigate the role of platelet activating factor (PAF) in myocardial ischaemia by using BN 50739, a new specific PAF receptor antagonist with a hetrazepine framework. DESIGN: Isolated working rat hearts were subjected to regional ischaemia, induced by ligation of the left main coronary artery for 30 min, followed by reperfusion. BN 50739 was applied at concentrations of 10(-7), 10(-6), 10(-5) and 5 X 10(-5) M, and its effects on the incidence of ischaemia induced and reperfusion induced ventricular tachycardia and ventricular fibrillation and heart functions, such as heart rate, coronary flow, aortic flow, left ventricular developed pressure (LVDP), its first derivative (LVdP/dtmax), and left ventricular end diastolic pressure (LVEDP), were determined. EXPERIMENTAL MATERIAL: Studies were performed on isolated working hearts of male Sprague-Dawley rats weighing 300-360 g. Hearts were perfused with BN 50739 dissolved in dimethylsulphoxide. Control hearts were perfused with the vehicle. MEASUREMENTS AND MAIN RESULTS: Regional ischaemia triggered ventricular arrhythmias showing high incidence between 12 and 20 min with peak appearance at 16 min. BN 50739 induced dose dependent protection against ventricular tachycardia and fibrillation: incidences declined from their respective control values of 91% and 75% to 33% (p less than 0.05) and 8% (p less than 0.05) after exposure to 10(-5) M, and to 25% (p less than 0.05) and 8% (p less than 0.05) after exposure to 5 X 10(-5) M concentrations. Reperfusion of the ischaemic myocardium resulted in an immediate appearance of ventricular tachycardia and fibrillation, but these were not suppressed by the PAF antagonist. Regional ischaemia slightly reduced heart rate, markedly decreased coronary flow, aortic flow, LVDP and LVdP/dtmax, and increased LVEDP. With the exception of LVEDP, these variables were not influenced by the drug. BN 50739, applied at a concentration of 5 X 10(-5) M, reduced LVEDP significantly during the whole ischaemic period. CONCLUSIONS: Under in vitro conditions PAF is likely to be involved in the genesis of ischaemia induced ventricular arrhythmias since BN 50739, a specific PAF receptor antagonist, exerts a protective effect against these rhythm disturbances. This suggests that PAF antagonists may have benefit in the clinical management of acute myocardial ischaemia.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research. - 25 : 5 (1991), p. 391-397. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Hosford, David Esanu, Andre Braquet, Pierre
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7.

001-es BibID:BIBFORM041652
035-os BibID:PMID:2759177
Első szerző:Koltai Mátyás
Cím:Ginkgolide B protects isolated hearts against arrhythmias induced by ischemia but not reperfusion / Mátyás Koltai, Árpád Tosaki, David Hosford, Pierre Braquet
Dátum:1989
Megjegyzések:The effect of ginkgolide B (BN 52021), a specific platelet-activating factor (PAF) antagonist, applied in doses of 1.5, 3.0, 6.0 X 10(-5) and 1.2 X 10(-4) mol/l, in comparison to that of metoprolol (10(-5) mol/l) and diltiazem (10(-7) mol/l), two widely used antiarrhythmic agents, on ischemia- and reperfusion-induced arrhythmias and heart functions, such as heart rate (HR), coronary flow (CF), aortic flow (AF), left ventricular developed pressure (LVDP), its first derivative (LVdp/dtmax), and left ventricular end-diastolic pressure (LVEDP) in isolated working rat hearts was examined. BN 52021 caused a dose-related protection against dysrhythmias, such as ventricular fibrillation, ventricular tachycardia, and premature ventricular beats induced by ischemia (30 min ligation of the left anterior descending coronary artery). The antiarrhythmic effect of BN 52021 given in a dose of 6.0 X 10(-5) mol/l was comparable to that of diltiazem and superior to the activity of metoprolol. None of the drugs influenced reperfusion-induced rhythm disturbances. BN 52021 did not alter heart functions, while metoprolol reduced (LVEDP only, and diltiazem increased CF, decreased AF, LVDP, and LVdp/dtmax during regional ischemia, indicating a negative inotropic effect. The antiarrhythmic effect of BN 52021 appears to be related to an antagonism of an increase in slow calcium influx induced by PAF in myocardial cells. Similarly to the mechanism of action of established antiarrhythmic drugs, BN 52021 can presumably prevent the re-entry mechanism involved in the development of ischemia-induced rhythm disturbances.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:European Journal of Pharmacology 164 : 2 (1989), p. 293-302. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Hosford, David Braquet, Pierre
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8.

001-es BibID:BIBFORM041644
Első szerző:Koltai Mátyás
Cím:PAF antagonists as potential therapeutic agents in cardiac anaphylaxis and myocardial ischemia / Matyas Koltai, Arpad Tosaki, Jean-Michel Guillon, David Hosford, Pierre Braquet
Dátum:1989
ISSN:0897-5957
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Drug Reviews 7 : 3 (1989), p. 177-198. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Guillon, Jean-Michel Hosford, David Braquet, Pierre
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9.

001-es BibID:BIBFORM041627
035-os BibID:PMID:2938453
Első szerző:Koltai Mátyás
Cím:Glucocorticoids in myocardial and cerebral infarction / M. Koltai, Á. Tósaki, I. Leprán, L. Szekeres
Dátum:1986
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Agents and Actions 17 : 3-4 (1986), p. 278-283. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Leprán István Szekeres László
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10.

001-es BibID:BIBFORM041626
035-os BibID:PMID:6548971
Első szerző:Koltai Mátyás
Cím:Prevention by macrocortin of global cerebral ischemia in Sprague-Dawley rats / Mátyás Koltai, Árpád Tósaki, Géza Adám, Ferenc Joó, György Nemecz, László Szekeres
Dátum:1984
Megjegyzések:We have previously shown that dexamethasone protects female Sprague-Dawley CFY rats against global cerebral ischemia induced by bilateral carotid artery ligation. In the present study, macrocortin derived from rat peritoneal cells exposed to dexamethasone was found to exhibit antiphospholipase A2 activity and to provide significant protection against the fatal consequences of carotid artery ligation. These results suggest that the cerebroprotective effect of glucocorticoids may be related to macrocortin production.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Pharmacology 105 : 3-4 (1984), p. 347-350. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Ádám Géza Joó Ferenc (1949-) (vegyész) Nemecz György Szekeres László
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11.

001-es BibID:BIBFORM041659
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effect of Cicletanine on Reperfusion-Induced Arrhythmias and Ion Shifts in Isolated Rat Hearts / Tosaki A., Koltai M., Willoughby D. A., Braquet P.
Dátum:1990
ISSN:0160-2446
Megjegyzések:Isolated hearts from normotensive (NT) and spontaneously hypertensive (SH) rats, subjected to normothermic global ischemia, were used to study whether cicletanine (a new antihypertensive drug) treatment exerts an antiarrhythmic effect against reperfusion-induced arrhythmias. The effect of the drug on myocardial ion contents (Na+, K+, Ca2+, and Mg2+) during ischemia and reperfusion was also determined. Using the optimal doses of cicletanine (30 and 100 mg/kg orally for 14 days), the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT) was reduced from their control values of 91 and 100% (after 30 min of ischemia) to 41 (p less than 0.05), 50 (p less than 0.05) and 41 (p less than 0.05), 58% in the NT group, while the corresponding value in the SH group for VF and VT were 17 (p less than 0.001), 33 (p less than 0.01) and 17 (p less than 0.001), 25% (p less than 0.001), respectively. The results obtained indicate that the cardioprotective effect of cicletanine was greater in the SH group than in the NT group. Cicletanine significantly reduced the ischemia- and reperfusion-induced myocardial Na+ and Ca2+ gains and inhibited the loss of myocardial K+ and Mg2+ in both NT and SH groups. The antiarrhythmic effect of cicletanine appears to be correlated with the preservation of myocardial Na+, K+, Ca2+, and Mg2+ contents via an ion transport modulation.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cardiovascular Pharmacology. - 15 : 2 (1990), p. 218-226. -
További szerzők:Koltai Mátyás Willoughby, Derek A. Braquet, Pierre
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12.

001-es BibID:BIBFORM041653
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effect of iloprost on reperfusion-induced arrhythmias and myocardial ion shifts in isolated rat hearts / Tosaki A., Koltai M., Paubert-Braquet M.
Dátum:1990
Megjegyzések:Isolated hearts excised from normotensive (NT) and spontaneously hypertensive (SH) rats subjected to transient normothermic global ischemia were used to study the effect of chronic treatment with iloprost on reperfusion-induced arrhythmias and myocardial ion shifts. After 30 min of ischemia, iloprost given s.c. in doses of 10, 50, 100 and 200 micrograms/kg per day for 14 days reduced the incidence of reperfusion-induced ventricular fibrillation (VF) in isolated hearts from the control value of 91 to 83, 75, 50 (P less than 0.05) and 25% (P less than 0.01) respectively, in NT rats. In the SH groups, the incidence of VF was also reduced from 100 to 75, 58, 33 (P less than 0.01) and 17% (P less than 0.001), respectively, with 10, 50, 100 and 200 micrograms/kg per day of iloprost. A similar reduction was observed in the incidence of reperfusion-induced ventricular tachycardia (VT). Ischemia and reperfusion caused significant changes in myocardial ion contents, i.e. an increase in Na+ and Ca2+ and a decrease in K+ and Mg2+ concentrations. The myocardial water content was also increased in parallel to the Na+ gain. The effect of iloprost given s.c. in doses of 50 and 200 micrograms/kg per day for 14 days was also measured on myocardial ion contents after 15- or 30-min ischemia and 30-min ischemia plus 10-min reperfusion. The higher iloprost dose significantly reduced the myocardial Na+, Ca2+ and water gains and the loss of K+ induced by ischemia and reperfusion in the NT and SH groups, while the decrease in Mg2+ content was alleviated only in SH rats. The results suggest that long-term iloprost treatment reduces the incidence of reperfusion-induced VF and VT by preventing Na+, Ca2+ and water accumulation as well as K+ and Mg2+ loss from myocardial tissue.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 191 : 1 (1990), p. 69-81. -
További szerzők:Koltai Mátyás Paubert-Braquet, M.
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